JNC 7 Express: The Seventh Report of the Joint National Committe on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

National High Blood Pressure Education Program

Complete Report

The Seventh Report of the Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

U . S . D E P A R T M E N T O F H E A LT H A N D H U M A N S E R V I C E S National Institutes of Health National Heart, Lung, and Blood Institute

Complete Report

The Seventh Report of the Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Heart, Lung, and Blood Institute National High Blood Pressure Education Program NIH Publication No. 04-5230 August 2004

This work was supported entirely by the National Heart, Lung, and Blood Institute. The Executive Committee, writing teams, and reviewers served as volunteers without remuneration.

Chair Aram V. Chobanian, M.D. (Boston University School of Medicine, Boston, MA) Executive Committee George L. Bakris, M.D. (Rush University Medical Center, Chicago, IL); Henry R. Black, M.D. (Rush University Medical Center, Chicago, IL); William C. Cushman, M.D. (Veterans Affairs Medical Center, Memphis, TN); Lee A. Green, M.D., M.P.H. (University of Michigan, Ann Arbor, MI); Joseph L. Izzo, Jr., M.D. (State University of New York at Buffalo School of Medicine, Buffalo, NY); Daniel W. Jones, M.D. (University of Mississippi Medical Center, Jackson, MS); Barry J. Materson, M.D., M.B.A. (University of Miami, Miami, FL); Suzanne Oparil, M.D. (University of Alabama at Birmingham, Birmingham, AL); Jackson T. Wright, Jr., M.D., Ph.D. (Case Western Reserve University, Cleveland, OH) Executive Secretary Edward J. Roccella, Ph.D., M.P.H. (National Heart, Lung, and Blood Institute, Bethesda, MD) Financial Disclosures Dr. Chobanian has received honoraria for serving as a speaker from Monarch, Wyeth, AstraZeneca, Solvay, and Bristol-Myers Squibb. Dr. Bakris has received honoraria for serving as a speaker from Astra-Zeneca, Abbott, Alteon, Biovail, Boerhinger-Ingelheim, Bristol-Myers Squibb, Forest, GlaxoSmithKline, Merck, Novartis, Sanofi, Sankyo, and Solvay; he has received funding/grant support for research projects from National Institutes of Health, AstraZeneca, Abbott, Alteon, Boerhinger-Ingelheim, Forest, GlaxoSmithKline, Merck, Novartis, Sankyo, and Solvay; he has served as a consultant/advisor for Astra-Zeneca, Abbott, Alteon, Biovail, Boerhinger-Ingelheim, Bristol-Myers Squibb, Forest, GlaxoSmithKline, Merck, Novartis, Sanofi, Sankyo, and Solvay. Dr. Black has received honoraria for serving as a speaker from Astra-Zeneca, Bristol-Myers Squibb, Novartis, Pfizer, Pharmacia, and Wyeth-Ayerst; he

has received funding/grant support for research projects from Bristol-Myers Squibb, BoehringerIngelheim, Merck, Pfizer, and Pharmacia; he has served as a consultant/advisor for Abbott, AstraZeneca, Biovail, Bristol-Myers Squibb, GlaxoSmithKline, Merck, Pfizer, and Pharmacia. Dr. Carter has served as a consultant/advisor for Bristol-Myers Squibb. Dr. Cushman has received funding/grant support for research projects from Astra-Zeneca, Merck, Pfizer, Kos, Aventis Pharma, King Pharmaceuticals, GlaxoSmithKline, and Boehringer-Ingelheim; he has served as a consultant/advisor for Bristol-Myers Squibb, Sanofi, GlaxoSmithKline, Novartis, Pfizer, Solvay, Pharmacia, Takeda, Sankyo, Forest, and Biovail. Dr. Izzo has received honoraria for serving as a speaker from Boehringer-Ingelheim, Merck, Pfizer, Astra-Zeneca, Solvay, Novartis, Forest, and Sankyo; he has received funding/grant support for research projects from Boehringer-Ingelheim, Merck, Astra-Zeneca, Novartis, GlaxoSmithKline, and Biovail; he served as a consultant/advisor for Merck, Astra-Zeneca, Novartis, Intercure, Sankyo, and Nexcura; he has stock holdings in Intercure, Nexcura. Dr. Jones has served as a consultant/advisor for Pfizer, Bristol-Myers Squibb, Merck, Forest, and Novartis. Dr. Manger has served as a consultant/advisor for the NHBPEP Coordinating Committee. Dr. Materson has served as a consultant/advisor for Unimed, Merck, GlaxoSmithKline, Novartis, Reliant, Tanabe, Bristol-Myers Squibb, Pfizer, Pharmacia, Noven, Boehringer-Ingelheim, and Solvay. Dr. Oparil has received funding/grant support for research projects from Abbott Laboratories, Astra-Zeneca, Aventis, Boehringer-Ingelheim, Bristol-Myers Squibb, Eli Lilly, Forest, GlaxoSmithKline, Monarch, Novartis [Ciba], Merck, Pfizer, Sanofi/BioClin, Schering Plough, Schwarz Pharma, Scios Inc, GD Searle, Wyeth-

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

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Ayerst, Sankyo, Solvay, and Texas Biotechnology Corporation; she has served as a consultant/advisor for Bristol-Myers Squibb, Merck, Pfizer, Sanofi, Novartis, The Salt Institute, and WyethAyerst; she is also on the Board of Directors for the Texas Biotechnology Corporation. Dr. Sowers has received honoraria for serving as a speaker from Med Com Vascular Biology Working Group and Joslin Clinic Foundation; he has received funding/grant support for research projects from Novartis and Astra-Zeneca. Dr. Wright has received honoraria for serving as a speaker from Astra, Aventis, Bayer, Bristol-Myers Squibb, Forest, Merck, Norvartis, Pfizer, Phoenix Pharmaceuticals, GlaxoSmithKline, and Solvay/Unimed; he has received funding/grant support for research projects from Astra, Aventis, Bayer, Biovail, Bristol-Myers Squibb, Forest, Merck, Norvartis, Pfizer, Phoenix Pharmaceuticals, GlaxoSmithKline, and Solvay/Unimed.

National High Blood Pressure Education Program Coordinating Committee Claude Lenfant, M.D. (National Heart, Lung, and Blood Institute, Bethesda, MD); George L. Bakris, M.D. (Rush University Medical Center, Chicago, IL); Henry R. Black, M.D. (Rush University Medical Center, Chicago, IL); Vicki Burt, Sc.M., R.N. (National Center for Health Statistics, Hyattsville, MD); Barry L. Carter, Pharm.D., F.C.C.P. (University of Iowa, Iowa City, IA); Francis D. Chesley, Jr., M.D. (Agency for Healthcare Research and Quality, Rockville, MD); Jerome D. Cohen, M.D. (Saint Louis University School of Medicine, St. Louis, MO); Pamela J. Colman, D.P.M. (American Podiatric Medical Association, Bethesda, MD); William C. Cushman, M.D. (Veterans Affairs Medical Center, Memphis, TN); Mark J. Cziraky, Pharm.D., F.A.H.A. (Health Core, Inc., Newark, DE); John J. Davis, P.A.-C. (American Academy of Physician Assistants, Memphis, TN); Keith Copelin Ferdinand, M.D., F.A.C.C. (Heartbeats Life Center, New Orleans, LA); Ray W. Gifford, Jr., M.D., M.S. (Cleveland Clinic Foundation, Fountain Hills, AZ); Michael Glick, D.M.D. (New Jersey Dental

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School, Newark, NJ); Lee A. Green, M.D., M.P.H. (University of Michigan, Ann Arbor, MI); Stephen Havas, M.D., M.P.H., M.S. (University of Maryland School of Medicine, Baltimore, MD); Thomas H. Hostetter, M.D. (National Institutes of Diabetes and Digestive and Kidney Diseases, Bethesda, MD); Joseph L. Izzo, Jr., M.D. (State University of New York at Buffalo School of Medicine, Buffalo, NY); Daniel W. Jones, M.D. (University of Mississippi Medical Center, Jackson, MS); Lynn Kirby, R.N., N.P., C.O.H.N. (Sanofi-Synthelabo Research, Malvern, PA); Kathryn M. Kolasa, Ph.D., R.D., L.D.N. (Brody School of Medicine at East Carolina University, Greenville, NC); Stuart Linas, M.D. (University of Colorado Health Sciences Center, Denver, CO); William M. Manger, M.D., Ph.D. (New York University Medical Center, New York, NY); Edwin C. Marshall, O.D., M.S., M.P.H. (Indiana University School of Optometry, Bloomington, IN); Barry J. Materson, M.D., M.B.A. (University of Miami, Miami, FL); Jay Merchant, M.H.A. (Centers for Medicare & Medicaid Services, Washington, DC); Nancy Houston Miller, R.N., B.S.N. (Stanford University School of Medicine, Palo Alto, CA); Marvin Moser, M.D. (Yale University School of Medicine, Scarsdale, NY); William A. Nickey, D.O. (Philadelphia College of Osteopathic Medicine, Philadelphia, PA); Suzanne Oparil, M.D. (University of Alabama at Birmingham, Birmingham, AL); Otelio S. Randall, M.D., F.A.C.C. (Howard University Hospital, Washington, DC); James W. Reed, M.D., F.A.C.P., F.A.C.E. (Morehouse School of Medicine, Atlanta, GA); Edward J. Roccella, Ph.D., M.P.H. (National Heart, Lung, and Blood Institute, Bethesda, MD); Lee Shaughnessy (National Stroke Association, Englewood, CO); Sheldon G. Sheps, M.D. (Mayo Clinic, Rochester, MN); David B. Snyder, R.Ph., D.D.S. (Health Resources and Services Administration, Rockville, MD); James R. Sowers, M.D., F.A.C.P., F.A.C.E. (SUNY Health Science Center at Brooklyn, Brooklyn, NY); Leonard M. Steiner, M.S., O.D. (Eye Group, Oakhurst, NJ); Ronald Stout, M.D., M.P.H. (Procter and Gamble, Mason, OH); Rita D. Strickland, Ed.D., R.N. (New York Institute of Technology,

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Springfield Gardens, NY); Carlos Vallbona, M.D. (Baylor College of Medicine, Houston, TX); Howard S. Weiss, M.D., M.P.H. (Georgetown University Medical Center, Washington Hospital Center, Walter Reed Army Medical Center, Washington, DC); Jack P. Whisnant, M.D. (Mayo Clinic and Mayo Medical School, Rochester, MN); Laurie Willshire, M.P.H., R.N. (American Red Cross, Falls Church, VA); Gerald J. Wilson, M.A., M.B.A. (Citizens for Public Action on Blood Pressure and Cholesterol, Inc., Potomac, MD); Mary Winston, Ed.D., R.D. (American Heart Association, Dallas, TX); Jackson T. Wright, Jr., M.D., Ph.D. (Case Western Reserve University, Cleveland, OH)

Additional Contributors Jan N. Basile, M.D., F.A.C.P. (Veterans Administration Hospital, Charleston, SC); James I. Cleeman, M.D. (National Heart, Lung, and Blood Institute, Bethesda, MD); Darla E. Danford, M.P.H, D.Sc. (National Heart, Lung, and Blood Institute, Bethesda, MD); Richard A. Dart, M.D., F.A.C.P., F.C.C.P., F.A.H.A. (Marshfield Clinic, Marshfield, WI); Karen A. Donato, S.M., R.D. (National Heart, Lung, and Blood Institute, Bethesda, MD); Mark E. Dunlap, M.D. (Louis Stokes Cleveland VA Medical Center, Cleveland, OH); Brent M. Egan, M.D. (Medical University of South Carolina, Charleston, SC); William J. Elliott, M.D., Ph.D. (Rush University Medical Center, Chicago, IL); Bonita E. Falkner, M.D. (Thomas Jefferson University, Philadelphia, PA); John M. Flack, M.D., M.P.H. (Wayne State University School of Medicine, Detroit, MI); David Lee Gordon, M.D. (University of Miami School of Medicine, Miami, FL); Philip B. Gorelik, M.D., M.P.H., F.A.C.P. (Rush Medical College, Chicago, IL); Mary M. Hand, M.S.P.H., R.N (National Heart, Lung, and Blood Institute, Bethesda, MD); Linda A. Hershey, M.D., Ph.D. (VA WNY Healthcare System, Buffalo, NY); Norman M. Kaplan, M.D. (University of Texas Southwestern Medical School at Dallas, Dallas, TX); Daniel Levy, M.D. (National Heart, Lung, and Blood Institute, Framingham, MA); James W. Lohr, M.D. (VA WNY Healthcare System and SUNY Buffalo, Buffalo, NY);

Vasilios Papademetriou, M.D., F.A.C.P., F.A.C.C. (Veterans Affairs Medical Center, Washington, DC); Thomas G. Pickering, M.D., D.Phil. (Mount Sinai Medical Center, New York, NY); Ileana L. Piña, M.D., F.A.C.C. (University Hospitals of Cleveland, Cleveland, OH); L. Michael Prisant, M.D., F.A.C.C., F.A.C.P. (Medical College of Georgia, Augusta, GA); Clive Rosendorff, M.D., Ph.D., F.R.C.P. (Veterans Affairs Medical Center, Bronx, NY); Virend K. Somers, M.D., Ph.D. (Mayo Clinic and Mayo Foundation, Rochester, MN); Ray Townsend, M.D. (University of Pennsylvania School of Medicine, Philadelphia, PA); Humberto Vidaillet, M.D. (Marshfield Clinic, Marshfield, WI); Donald G. Vidt, M.D. (Cleveland Clinic Foundation, Cleveland, OH); William White, M.D. (The University of Connecticut Health Center, Farmington, CT)

Staff Joanne Karimbakas, M.S., R.D. (American Institutes for Research Health Program, Silver Spring, MD) We appreciate the assistance by: Carol Creech, M.I.L.S. and Gabrielle Gessner (American Institutes for Research Health Program, Silver Spring, MD).

National High Blood Pressure Education Program Coordinating Committee Member Organizations American Academy of Family Physicians American Academy of Neurology American Academy of Ophthalmology American Academy of Physician Assistants American Association of Occupational Health Nurses American College of Cardiology American College of Chest Physicians American College of Occupational and Environmental Medicine American College of Physicians-American Society of Internal Medicine American College of Preventive Medicine American Dental Association American Diabetes Association American Dietetic Association American Heart Association American Hospital Association

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American Medical Association American Nurses Association American Optometric Association American Osteopathic Association American Pharmaceutical Association American Podiatric Medical Association American Public Health Association American Red Cross American Society of Health-System Pharmacists American Society of Hypertension American Society of Nephrology Association of Black Cardiologists Citizens for Public Action on High Blood Pressure and Cholesterol, Inc. Hypertension Education Foundation, Inc. International Society on Hypertension in Blacks National Black Nurses Association, Inc. National Hypertension Association, Inc. National Kidney Foundation, Inc. National Medical Association National Optometric Association National Stroke Association National Heart, Lung, and Blood Institute Ad Hoc Committee on Minority Populations Society for Nutrition Education The Society of Geriatric Cardiology Federal Agencies: Agency for Health Care Research and Quality Centers for Medicare & Medicaid Services Department of Veterans Affairs Health Resources and Services Administration National Center for Health Statistics National Heart, Lung, and Blood Institute National Institute of Diabetes and Digestive and Kidney Diseases

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The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Contents

Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiv Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Lifetime Risk of Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Blood Pressure and Cardiovascular Risk. . . . . . . . . . . . . . . . . . . . . . . . . 9 Basis for Reclassification of Blood Pressure . . . . . . . . . . . . . . . . . . . . . 11 Classification of Blood Pressure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Cardiovascular Disease Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Importance of Systolic Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . 14 Prevention of Hypertension: Public Health Challenges . . . . . . . . . . . . 16 Community Programs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Calibration, Maintenance, and Use of Blood Pressure Devices. . . . . . 18 Accurate Blood Pressure Measurement in the Office. . . . . . . . . . . . . . . 18 Ambulatory Blood Pressure Monitoring. . . . . . . . . . . . . . . . . . . . . . . . 19 Self-Measurement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

Patient Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Laboratory Tests and Other Diagnostic Procedures . . . . . . . . . . . . . . . 21

Identifiable Causes of Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Genetics of Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Blood Pressure Control Rates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Goals of Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Benefits of Lowering Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Lifestyle Modifications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Pharmacologic Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Rationale for Recommendation of Thiazide-Type Diuretics as Preferred Initial Agent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 Achieving Blood Pressure Control in Individual Patients. . . . . . . . . . . . 30 Followup and Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

Special Situations in Hypertension Management . . . . . . . . . . . . . . . . 33 Compelling Indications . . . . . . . . . . . . . . Ischemic Heart Disease . . . . . . . . . . . . Heart Failure . . . . . . . . . . . . . . . . . . . Diabetes and Hypertension . . . . . . . . . Chronic Kidney Disease . . . . . . . . . . . Patients With Cerebrovascular Disease Other Special Situations . . . . . . . . . . . . . Minorities . . . . . . . . . . . . . . . . . . . . . Metabolic Syndrome. . . . . . . . . . . . . .

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Prevelance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Age Trends . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Clinical Impact . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Clinical Management of the Metabolic Syndrome . . . . . . . . . . . . . . 41 Lipids. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Overweight and Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Left Ventricular Hypertrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Peripheral Arterial Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Hypertension in Older People . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 Orthostatic Hypotension. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Resistant Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Cognitive Function and Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Hypertension in Women . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Hypertension in Children and Adolescents. . . . . . . . . . . . . . . . . . . . 53 Hypertensive Crises: Emergencies and Urgencies . . . . . . . . . . . . . . . 54 Erectile Dysfunction and Hypertension . . . . . . . . . . . . . . . . . . . . . . 54 Urinary Outflow Obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Patients Undergoing Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Dental Issues in Hypertensive Individuals . . . . . . . . . . . . . . . . . . . . 56 Obstructive Sleep Apnea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 Hypertension and the Eye . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 Renal Transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 Patients With Renovascular Disease . . . . . . . . . . . . . . . . . . . . . . . . 58

Drugs and Other Agents Affecting Blood Pressure. . . . . . . . . . . . . . . . 59 Alcohol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60 Nonaspirin Nonsteroidal Anti-Inflammatory Drugs . . . . . . . . . . . . . . . 60

Improving Hypertension Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Issues Dealing With Adherence to Regimens . . . . . . . . . . . . . . . . . . . . 61 What Can the Clinician Do? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Clinical Inertia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Role of Other Health Care Professionals . . . . . . . . . . . . . . . . . . . . . . . 62 Patient Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 Characterization of Patients Leading to Tailored Therapy . . . . . . . . 63 Goal Setting and Behavioral Change . . . . . . . . . . . . . . . . . . . . . . . . 63 Economic Barriers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 Additional Sources of Information. . . . . . . . . . . . . . . . . . . . . . . . . . . . 64

Scheme Used for Classification of the Evidence. . . . . . . . . . . . . . . . . . 65 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

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The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

L i s t o f Ta b l e s

Ta b l e 1 .

Trends in awareness, treatment, and control of high blood pressure, 1976–2000 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Ta b l e 2 .

Changes in blood pressure classification . . . . . . . . . . . . . . . . . 11

Ta b l e 3 .

Classification of blood pressure for adults. . . . . . . . . . . . . . . . 12

Ta b l e 4 .

Recommendations for followup based on initial blood pressure measurements for adults without acute end organ damage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Ta b l e 5 .

Clinical situations in which ambulatory blood pressure monitoring may be helpful . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

Ta b l e 6 .

Cardiovascular risk factors. . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Ta b l e 7 .

Identifiable causes of hypertension . . . . . . . . . . . . . . . . . . . . . 21

Ta b l e 8 .

Screening tests for identifiable hypertension . . . . . . . . . . . . . . 22

Ta b l e 9 .

Lifestyle modifications to prevent and manage hypertension . . 26

Ta b l e 1 0 . Oral antihypertensive drugs . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Ta b l e 1 1 . Combination drugs for hypertension. . . . . . . . . . . . . . . . . . . . 29 Ta b l e 1 2 . Clinical trial and guideline basis for compelling indications for individual drug classes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Ta b l e 1 3 . Clinical criteria defining the metabolic syndrome in Adult Treatment Panel III . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Ta b l e 1 4 . Estimated prevalence of the metabolic syndrome using the Adult Treatment Panel III definition among normal weight, overweight, and obese men and women in the National Health and Nutrition Examination Survey III . . . . . . 40 Ta b l e 1 5 . Relative 10-year risk for diabetes, hypertension, heart disease, and stroke over the next decade among men initially free of disease stratified by baseline body mass index. . . 42 Ta b l e 1 6 . Lifestyle changes beneficial in reducing weight . . . . . . . . . . . . 42 Ta b l e 1 7 . Medical therapies of peripheral arterial disease . . . . . . . . . . . . 44 Ta b l e 1 8 . Causes of resistant hypertension . . . . . . . . . . . . . . . . . . . . . . . 47 Ta b l e 1 9 . Classification of hypertension in pregnancy. . . . . . . . . . . . . . . 50 Ta b l e 2 0 . Treatment of chronic hypertension in pregnancy . . . . . . . . . . . 51 Ta b l e 2 1 . Treatment of acute severe hypertension in preeclampsia. . . . . . 52 Ta b l e 2 2 . The 95th percentile of blood pressure by selected ages, by the 50th and 75th height percentiles, and by gender in children and adolescents. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Ta b l e 2 3 . Parenteral drugs for treatment of hypertensive emergencies . . . 55 Ta b l e 2 4 . Common substances associated with hypertension in humans . . 59 Ta b l e 2 5 . Provide empathetic reinforcement . . . . . . . . . . . . . . . . . . . . . . 61

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Ta b l e 2 6 . Clinician awareness and monitoring . . . . . . . . . . . . . . . . . . . . 61 Ta b l e 2 7 . Organize care delivery systems . . . . . . . . . . . . . . . . . . . . . . . . 62 Ta b l e 2 8 . Patient education about treatment . . . . . . . . . . . . . . . . . . . . . 62 Ta b l e 2 9 . Collaborate with other health professionals . . . . . . . . . . . . . . 62 Ta b l e 3 0 . Individualize the regimen . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 Ta b l e 3 1 . Promote social support systems . . . . . . . . . . . . . . . . . . . . . . . 63

x

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

LIST

OF

FIGURES

Fi g u r e 1 .

Smoothed weighted frequency distribution, median, and 90th percentile of systolic blood pressure for ages 60–74 years: United States, 1960–1991. . . . . . . . . . . . . . . . . 2

Fi g u r e 2 .

Percent decline in age-adjusted mortality rates for stroke by gender and race: United States, 1970–2000 . . . . . . . . . . . . . . 2

Fi g u r e 3 .

Percent decline in age-adjusted mortality rates for coronary heart disease by gender and race: United States, 1970–2000. . . 3

Fi g u r e 4 .

Hospital case-fatality rates for congestive heart failure for ages younger than 65 years and 65 years and older: United States, 1981–2000 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Fi g u r e 5 .

Prevalence of congestive heart failure by race and gender, ages 25–74 years: United States, 1971–74 to 1999–2000 . . . . 4

Fi g u r e 6 .

Hospitalization rates for congestive heart failure, ages 45–64 years and 65 years and older: United States, 1971–2000 . . . . 5

Fi g u r e 7 .

Trends in incident rates of end-stage renal disease, by primary diagnosis (adjusted for age, gender, race) . . . . . . . . . 5

Fi g u r e 8 .

Residual lifetime risk of hypertension in women and men aged 65 years . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Fi g u r e 9 .

Ischemic heart disease mortality rate in each decade of age versus usual blood pressure at the start of that decade . . . 9

Fi g u r e 1 0 . Stroke mortality rate in each decade of age versus usual blood pressure at the start of that decade . . . . . . . . . . . . . . 10 Fi g u r e 1 1 . Impact of high normal blood pressure on the risk of cardiovascular disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Fi g u r e 1 2 . Ten-year risk for coronary heart disease by systolic blood pressure and presence of other risk factors. . . . . . . . . . . . . . 13 Fi g u r e 1 3 . Changes in systolic and diastolic blood pressure with age . . 14 Fi g u r e 1 4 . Difference in coronary heart disease prediction between systolic and diastolic blood pressure as a function of age . . . 15 Fi g u r e 1 5 . Systolic blood pressure distributions . . . . . . . . . . . . . . . . . . 16 Fi g u r e 1 6 . Algorithm for treatment of hypertension . . . . . . . . . . . . . . . 31 Fi g u r e 1 7 . Frequency distribution of untreated hypertensive individuals by age and hypertension subtype . . . . . . . . . . . . 44

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

xi

Foreword

The complete version of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7) provides additional scientific evidence to bolster other JNC 7 products: the JNC 7 Express; Facts About the DASH Eating Plan; Your Guide to Lowering High Blood Pressure; Reference Card from the JNC 7 for clinicians; Blood Pressure Wallet Card for patients; and Palm application of the JNC 7 recommendations. These educational materials are available on the NHLBI Web site http://www.nhlbi.nih.gov/. The purpose of JNC reports is to synthesize the available scientific evidence and offer guidance to busy primary care clinicians. Readers of this report should remember that this document is intended as a guide, not a mandate. The National High Blood Pressure Education Program (NHBPEP) recognizes the responsible clinician’s judgment regarding the management of patients remains paramount. Therefore, JNC documents are tools to be adopted and implemented in local and individual settings. In the production of this report, much discussion was generated regarding the interpretation of the available scientific literature. However, after all of the discussions within the JNC 7 Executive Committee and the NHBPEP Coordinating Committee, as well as the many discussions at conferences and scientific meetings conducted in the United States and worldwide, the conclusion is that best management practice occurs when hypertension is treated to goal levels and blood pressure control is sustained over time. This is irrefutable but, unfortunately, hypertension treatment and

control rates worldwide are simply not as good as they could be. By developing this stellar landmark report, Dr. Aram Chobanian, the JNC 7 Executive Committee, and members of the NHBPEP Coordinating Committee, as well as the writers and the contributors to this document, have addressed the important public health issue of improving inadequate blood pressure control. Applying JNC 7 recommendations to clinical practice will prevent the devastating consequences of uncontrolled hypertension. I recommend this guideline to clinicians and public health workers with the conviction that its contents will indeed contribute to the further prevention of premature morbidity and mortality. Dr. Chobanian has our deep gratitude for leading the effort to develop this report in such a timely manner. His brilliant leadership is what made the JNC 7 and related materials possible. The NHBPEP will release other advisories as the scientific evidence becomes available.

Barbara M. Alving, M.D. Acting Director National Heart, Lung, and Blood Institute and Chair National High Blood Pressure Education Program Coordinating Committee

Foreword

xiii

Abstract

The purpose of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are: in those older than age 50, systolic blood pressure (SBP) of >140 mmHg is a more important cardiovascular disease (CVD) risk factor than diastolic BP (DBP); beginning at 115/75 mmHg, CVD risk doubles for each increment of 20/10 mmHg; those who are normotensive at 55 years of age will have a 90 percent lifetime risk of developing hypertension; prehypertensive individuals (SBP 120–139 mmHg or DBP 80–89 mmHg) require healthpromoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific

xiv

high-risk conditions, which are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (115 mmHg SBP) is responsible for 62 percent of cerebrovascular disease and 49 percent of ischemic heart disease (IHD), with little variation by sex. In addition, suboptimal BP is the number one attributable risk factor for death throughout the world.3

Considerable success has been achieved in the past in meeting the goals of the program. The awareness of hypertension among Americans has improved from a level of 51 percent in the period 1976–1980 to 70 percent in 1999–2000 (table 1). The percentage of patients with hypertension receiving treatment has increased from 31 percent to 59 percent in the same period, and the percentage of persons with high BP controlled to below 140/90 mmHg has increased from 10 percent to 34 percent. Between 1960 and 1991, median SBP for individuals ages 60–74 declined by approximately 16 mmHg (figure 1). These changes have been associated with highly favorable trends in the morbidity and mortality attributed to hypertension. Since 1972, age-adjusted death rates from stroke and coronary heart disease (CHD) have declined by approximately 60 percent and 50 percent, respectively (figures 2 and 3). These benefits have occurred independent of gender, age, race, or socioeconomic status. Within the last two decades, better treatment of hypertension has been associated with a considerable reduction in the hospital case-fatality rate for heart failure (HF) (figure 4). This information suggests that there have been substantial improvements.

Table 1. Trends in awareness, treatment, and control of high blood pressure, 1976–2000* National Health and Nutrition Examination Survey, Percent 1976–801

1988–911

1991–942

1999–20003

Awareness

51

73

68

70

Treatment

31

55

54

59

Control†

10

29

27

34

* Percentage of adults ages 18 to 74 years with SBP of 140 mmHg or greater, DBP of 90 mmHg or greater, or taking antihypertensive medication. † SBP below 140 mmHg and DBP below 90 mmHg, and on antihypertensive medication.

Sources: 1

Data from Burt VL, et al. Prevalance of hypertension in the US adult population. Results from the Third National Health and Nutrition Examination Survey, 1988–1991. Hypertension 1995;26:60–9. 2 Data from The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;157:2413–46. 3 The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA 2003;289:2560–71. Introduction

1

Figure 1. Smoothed weighted frequency distribution, median, and 90th percentile of systolic blood pressure for ages 60–74 years: United States, 1960–1991 % 14

AGES 60 to 74

12 10 8

Median

6

90th percentile

4 2

220

210

200

190

180

170

160

150

140

130

120

110

100

90

80

70

0

mmHg

NHES I (1960–62) NHANES II (1976–80)

NHANES I (1971–74) NHANES III (1988–91)

NHANES, National Health and Nutrition Examination Survey; NHES, National Health Examination Survey Source: Burt VL, et al. Trends in the prevalance, awareness, treatment, and control of hypertension in the adult US population. Data from the health examination surveys, 1960 to 1991. Erratum in: Hypertension 1996;7(5):1192.

Figure 2. Percent decline in age-adjusted mortality rates for stroke by gender and race: United States, 1970–2000 10 0

P e r c e n t D ec l i n e

-10 -20 -30 -40 -50 -60 -70 1970

1975

1980

1985

1990

1995

2000

Ye a r

White men White women

Black men Black women

Source: Prepared by Thom T, National Heart, Lung, and Blood Institute from Vital Statistics of the United States, National Center for Health Statistics. Death rates are age-adjusted to the 2000 U.S. census population.

2

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Figure 3. Percent decline in age-adjusted mortality rates for coronary heart disease by gender and race: United States, 1970–2000 10 0

P e r c e n t D ec l i n e

-10 -20 -30 -40 -50 -60 -70 1970

1975

1980

1985

1990

1995

2000

Ye a r

White men White women

Black men Black women

Source: Prepared by Thom T, National Heart, Lung, and Blood Institute from Vital Statistics of the United States, National Center for Health Statistics. Death rates are age-adjusted to the 2000 U.S. census population.

Figure 4. Hospital case-fatality rates for congestive heart failure for ages younger than 65 years and 65 years and older: United States, 1981–2000 I n H o s pi ta l M o rta l i t y ( P e r c e n t )

14 12 10 8 6 4 2 0 1980

1985

1990

1995

2000

Ye a r

Ages 40 percent of individuals with hypertension are not on treatment, and two-thirds of hypertensive patients are not being controlled to BP levels 88 cm (>35 inches) for women

■

Blood pressure: >130 mmHg systolic and/or >85 mmHg diastolic

■

Fasting glucose: >110 mg/dL or 6.1 mmol/L

■

Triglycerides: >150 mg/dL or 1.69 mmol/L

■

HDL-cholesterol: 90 mmHg); ■ IDH (SBP 90 mmHg). Source: Franklin SS, et al. Predominance of isolated systolic hypertension among middle-aged and elderly US hypertensives. Analysis based on National Health and Nutrition Examination Survey (NHANES III). Hypertension 2001;37:869–74.

44

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

individuals have systolic hypertension and about three-fourths have ISH. Individuals over age 60 represent the most rapidly growing segment of the U.S. population, and even in those who remain normotensive between 55 and 65 years of age, there remains a lifetime risk of developing hypertension that exceeds 90 percent.16 At the same time, there is a three- to fourfold increase in CVD risk in older compared to younger individuals. These facts prompted the NHBPEP to issue a clinical advisory statement in May 2000 stating that SBP should be the primary target for the diagnosis and management of older people with hypertension.256 Currently, BP control rates (systolic 75 percent of women older than 75 years of age.295 Awareness, treatment, and control of high BP in women. Women are more likely than men to know that they have hypertension, to have it treated, and to have it controlled.1 In NHANES III, approximately 75 percent of hypertensive Black and White women were aware of their high BP in contrast to 65 percent of hypertensive men in these ethnic groups. Overall, 61 percent of hypertensive women, but only 44 percent of men, were being treated with antihypertensive medications. The higher treatment rates in women have been attributed to increased numbers of physician contact. Menopause and blood pressure. The effect of menopause on BP is controversial. Longitudinal studies have not documented a rise in BP with menopause, while cross-sectional studies have found significantly higher SBP and DBP in postmenopausal versus premenopausal women.294 In NHANES III, the rate of rise in SBP tended to be steeper in postmenopausal compared to premenopausal women until the sixth decade, when the rate of increase tended to slow. Staessen et al. reported that, even after adjustment for age and BMI, postmenopausal women are more than twice as likely to have hypertension as premenopausal women.296 In a prospective study of conventional and ambulatory BP levels,

48

postmenopausal women had higher SBP (4–5 mmHg) than pre- and perimenopausal controls.297 The increase in SBP per decade was 5 mmHg greater in the peri- and postmenopausal women than in the premenopausal group. Thus, there is evidence that at least part of the rise in BP (particularly SBP) seen later in life in women is due to menopause. A menopause-related increase in BP has been attributed to a variety of factors, including estrogen withdrawal, overproduction of pituitary hormones, weight gain, or a combination of these and other yet undefined neurohumoral influences.298 Postmenopausal hormone therapy and BP. Results of studies evaluating the effects of hormone replacement therapy (HRT) on BP have been inconsistent. The Women’s Health Initiative (WHI), the largest longitudinal study to address this question, found an average 1 mmHg increase in SBP over 5.6 years of followup among 8,506 postmenopausal women randomized to conjugated equine estrogen and medroxyprogesterone acetate as compared to a placebo group.299 There was no difference in DBP between the hormone treatment groups. Further, in the WHI crosssectional analysis of almost 100,000 women 50–79 years of age, current hormone use was associated with a >25 percent likelihood of having hypertension compared to past use or no prior use.300 Smaller observational and interventional studies have found different results. In the Baltimore Longitudinal Study on Aging (BLSA), women receiving HRT had a significantly smaller increase in SBP over time than nonusers, but DBP was not affected. The Postmenopausal Estrogen/Progestin Intervention trial showed no effect of HRT on SBP or DBP.301 In small studies that used 24-hour ABPM to evaluate the effects of HRT on BP, while overall results were inconsistent, several of the studies suggest that HRT improves or restores the normal nighttime reduction (“dipping”) in BP that may be diminished in postmenopausal women. Such an effect would tend to reduce total BP load and thereby reduce target organ damage.298 Overall, HRT-related change in BP is likely to be modest and should not preclude hormone use in normotensive or hypertensive women. All hyper-

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

tensive women treated with HRT should have their BP monitored closely at first and then at 6-month intervals. Oral contraceptives and BP. Many women taking oral contraceptives experience a small but detectable increase in BP; a small percentage experience the onset of frank hypertension. This is true even with modern preparations that contain only 30 µg estrogen. The Nurses’ Health Study found that current users of oral contraceptives had a significantly increased (relative risk [RR]=1.8; 95 percent confidence interval [CI]=1.5–2.3) risk of hypertension compared with those who had never used oral contraceptives.302 Absolute risk was small: only 41.5 cases of hypertension per 10,000 person/years could be attributed to oral contraceptive use. Controlled prospective studies have demonstrated a return of BP to pretreatment levels within 3 months of discontinuing oral contraceptives, indicating that their BP effect is readily reversible. Oral contraceptives occasionally may precipitate accelerated or malignant hypertension. Family history of hypertension, including preexisting pregnancy-induced hypertension, occult renal disease, obesity, middle age (>35 years), and duration of oral contraceptive use increase susceptibility to hypertension. Contraceptive-induced hypertension appears to be related to the progestogenic, not the estrogenic, potency of the preparation. Regular monitoring of BP throughout contraceptive therapy is recommended, and it has been suggested that contraceptive prescriptions be limited to 6 months to ensure at least semiannual reevaluations. Withdrawal of the offending contraceptive agent is generally desirable in cases of contraceptive-induced hypertension, but such therapy may have to be continued in some women (e.g., if other contraceptive methods are not suitable) and combined with antihypertensive therapy. Outcomes of antihypertensive trials in women. Relative benefits of antihypertensive therapy do not appear to differ between the sexes.303 Absolute risk reduction for stroke was also similar in men and women, but for coronary events, it was greater in men. Similarly, a placebo-

controlled trial of CCB treatment showed treatment benefits for both sexes.113,304 More recent outcome trials comparing ACEIs, ARBs, or CCBs to diuretics and BBs in older, high-risk patients have generally shown similar benefits for women and men.101,102,109 The current evidence indicates that the sex of the patient should not play a role in decisions about whether to treat high BP. Choice of antihypertensive drugs for women. While women generally respond to antihypertensive drugs similarly to men, some special considerations may dictate treatment choices for women. ACEIs and ARBs are contraindicated for women who are or intend to become pregnant because of the risk of fetal developmental abnormalities. Diuretics are particularly useful in elderly individuals because of a decreased risk of hip fracture. Some antihypertensive drugs have gender-specific adverse effect profiles. For example, in the TOMHS, women reported twice as many adverse effects as men.305 Women are more likely to develop diuretic-induced hyponatremia, and men are more likely to develop gout. Hypokalemia is more common in women taking a diuretic. ACEIinduced cough is twice as common in women as in men, and women are more likely to complain of CCB-related peripheral edema and minoxidilinduced hirsutism. Pregnant Women Hypertensive disorders in pregnancy are a major cause of maternal, fetal, and neonatal morbidity and mortality. Hypertension in pregnancy is classified into one of five categories (table 19), and it is critical to differentiate preeclampsia, a pregnancyspecific syndrome of exaggerated vasoconstriction and reduced organ perfusion, from pre-existing chronic hypertension.7,306 Prepregnancy assessment. Women should be evaluated prior to conception to define their BP status, and if hypertensive, to assess its severity, possible secondary causes, and presence of target organ damage, and to plan treatment strategies. Many hypertensive women who plan to become pregnant should be screened for pheochromocytoma due to the high morbidity and mortality of this condition if not diagnosed antepartum.

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49

Table 19. Classification of hypertension in pregnancy Chronic hypertension

■

■

Preeclampsia

■

■ ■

Chronic hypertension with superimposed preeclampsia

■ ■

■ ■ ■ ■

Gestational hypertension

■ ■ ■

■ ■

Transient hypertension

■ ■ ■ ■

BP >140 mmHg systolic or 90 mmHg diastolic prior to pregnancy or before 20 weeks gestation Persists >12 weeks postpartum BP >140 mmHg systolic or 90 mmHg diastolic with proteinuria (>300 mg/24 hrs) after 20 weeks gestation Can progress to eclampsia (seizures) More common in nulliparous women, multiple gestation, women with hypertension for >4 years, family history of preeclampsia, hypertension in previous pregnancy, renal disease New onset proteinuria after 20 weeks in a woman with hypertension In a woman with hypertension and proteinuria prior to 20 weeks gestation Sudden two- to threefold increase in proteinuria Sudden increase in BP Thrombocytopenia Elevated AST or ALT Hypertension without proteinuria occurring after 20 weeks gestation Temporary diagnosis May represent preproteinuric phase of preeclampsia or recurrence of chronic hypertension abated in midpregnancy May evolve to preeclampsia If severe, may result in higher rates of premature delivery and growth retardation than mild preeclampsia Retrospective diagnosis BP normal by 12 weeks postpartum May recur in subsequent pregnancies Predictive of future primary hypertension

ALT, alanine aminotransferase; AST, aspartate aminotransaminase; BP, blood pressure

In hypertensive women planning to become pregnant, it may be prudent prior to conception to change to antihypertensive medications known to be safe during pregnancy, such as methyldopa or BBs. ACEIs and ARBs should be discontinued prior to attempts at conception or as soon as pregnancy is confirmed. Those with progressive renal diseases should be encouraged to complete their childbearing while their renal function is relatively well preserved. Mild renal disease (serum creatinine 1.4 mg/dL at conception. Antihypertensive drug selection. The primary goal of treating chronic hypertension in pregnancy is to reduce maternal risk, but the choice of antihypertensive agent(s) is largely driven by the safety of the fetus. Methyldopa is preferred by many as first-line therapy, based on reports of stable uteroplacental blood flow and fetal hemodynamics and the absence of long-term (7.5-year followup) adverse effects on development of children exposed to methyldopa in utero.309,310 Other treatment options are summarized in table 20. Preeclampsia. Preeclampsia is more common in women with chronic hypertension, with an incidence of approximately 25 percent. Risk factors for superimposed preeclampsia include renal insufficiency, a history of hypertension for 4 years or longer, and hypertension in a previous pregnancy. Prevention of preeclampsia relies on: (1) identification of high-risk women; (2) close clinical and laboratory monitoring aimed at its early recognition; and

Table 20. Treatment of chronic hypertension in pregnancy Agent

Comments

Methyldopa

■

Preferred based on long-term followup studies supporting safety

BBs

■

Reports of intrauterine growth retardation (atenolol) Generally safe

■

Labetalol

■

Increasingly preferred to methyldopa due to reduced side effects

Clonidine

■

Limited data

Calcium antagonists

■

Limited data No increase in major teratogenicity with exposure

■

Diuretics

■ ■

ACEIs, angiotensin II receptor antagonists

■ ■

Not first-line agents Probably safe Contraindicated Reported fetal toxicity and death

ACEIs, angiotensin converting enzyme inhibitors; BBs, beta-blockers Special Situations in Hypertension Management

51

(3) institution of intensive monitoring or delivery when indicated. Treatment of preeclampsia includes hospitalization for bed rest, control of BP, seizure prophylaxis in the presence of signs of impending eclampsia, and timely delivery. Importantly, many women with preeclampsia have previously been normotensive, so acute BP elevations even to modest levels (i.e., 150/100 mmHg) may cause significant symptomatology and require treatment. Treatment does not alter the underlying pathophysiology of the disease, but it may slow its progression and provide time for fetal maturation. Preeclampsia rarely remits spontaneously and in most cases worsens with time. While delivery may be appropriate therapy for the mother, it may compromise a fetus of 20 mmHg above the 95th percentile). Chronic hypertension is becoming increasingly common in adolescence and is generally associated with obesity, sedentary lifestyle, and a positive family history of hypertension and other CVDs. As in adults, children and adolescents with established hypertension develop target organ damage including LVH. Appropriate assessment for LVH, including echocardiography, should be considered in children who have significant and persistant hypertension.

Lifestyle interventions should be recommended for all children with hypertension, with pharmacologic therapy instituted for higher levels of BP or if insufficient response to lifestyle modifications occurs. Teenage children with BP below but near the 95th percentile should adopt healthy lifestyles similar to adults with prehypertension. Although the recommendations for choice of drugs are generally similar in children and adults, dosages of antihypertensive medication for children should be smaller and adjusted very carefully. ACEIs and ARBs should not be used if the patient is pregnant. These agents should be used with extreme caution in sexually active teenage girls and only when careful counseling and effective pregnancy precautions are established. The presence of uncomplicated hypertension is not a reason to restrict children from participating in physical activities, particularly because exercise may lower BP. Use of anabolic steroid hormones for the purpose of bodybuilding should be strongly discouraged. Efforts should be made to identify other modifiable risk factors in children (e.g., obesity, lack of physical activity, smoking), and vigorous interventions should be made when these factors are present. Detailed recommendations regarding hypertension in children and adolescents can be found in the 1996 NHBPEP Working Group Report on Hypertension Control in Children and Adolescents.311

Table 22. The 95th percentile of blood pressure by selected ages, by the 50th and 75th height percentiles, and by gender in children and adolescents Girls’ SBP/DBP

Boys’ SBP/DBP

Age

50th Percentile for Height

75th Percentile for Height

50th Percentile for Height

75th Percentile for Height

1

104/58

105/59

102/57

104/58

6

111/73

112/73

114/74

115/75

12

123/80

124/81

123/81

125/82

17

129/84

130/85

136/87

138/88

DBP, diastolic blood pressure; SBP, systolic blood pressure Source: Adapted from the National High Blood Pressure Education Program. Update on the 1987 Task Force Report on High Blood Pressure in Children and Adolescents: A working group report from the National High Blood Pressure Education Program. National High Blood Pressure Education Program Working Group on Hypertension Control in Children and Adolescents. Pediatrics 1996;98(pt 1):649–58.

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Hypertensive Crises: Emergencies and Urgencies Hypertensive emergencies are characterized by severe elevations in BP (>180/120 mmHg) complicated by evidence of impending or progressive target organ dysfunction. They require immediate BP reduction (not necessarily to normal) to prevent or limit target organ damage.312,313 Examples include hypertensive encephalopathy, intracerebral hemorrhage, acute MI, acute left ventricular failure with pulmonary edema, unstable angina pectoris, dissecting aortic aneurysm, or eclampsia. Hypertensive urgencies are those situations associated with severe elevations in BP without progressive target organ dysfunction. Examples include upper levels of stage II hypertension associated with severe headache, shortness of breath, epistaxis, or severe anxiety. The majority of these patients present as noncompliant or inadequately treated hypertensive individuals, often with little or no evidence of target organ damage. Early triage to establish the appropriate therapeutic strategies for these patients is critical to limiting morbidity and mortality.314 Patients presenting with severe hypertension may represent as much as 25 percent of all patient visits to busy urban emergency rooms (ERs).315 Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of BP and parenteral administration of an appropriate agent (table 23). The initial goal of therapy in hypertensive emergencies is to reduce mean arterial BP by no more than 25 percent (within minutes to 1 hour), then if stable, to 160/100–110 mmHg within the next 2–6 hours. Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided. For this reason, short-acting nifedipine is no longer considered acceptable in the initial treatment of hypertensive emergencies or urgencies. If this level of BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented in the next 24–48 hours. There are exceptions to the above recommendation—patients with an ischemic stroke in which there is no clear evidence from clinical trials to support the use of immediate antihypertensive treatment, patients with

54

aortic dissection who should have their SBP lowered to 50 percent of individuals with OSA have hypertension.263,326–333 Obesity is so common in OSA that the index of suspicion for OSA should be high in any hypertensive patient whose BMI is above 27 kg/m2.331 These individuals should be questioned thoroughly for symptoms of OSA, including snoring, witnessed apnea, irregular breathing during sleep, restless sleeping, and chronic morning fatigue. Frequently it is the sleep partner who provides the most reliable history, especially regarding snoring, because the affected individual may deny or be unaware of the problem. If the diagnosis is suspected clinically, confirmation by a formal sleep study is indicated. The impact of sleep apnea on CVD is probably related in large part to its association with elevated BP. However, OSA may act through a number of mechanisms to elicit myocardial and vascular damage, including an increase in catecholamine release,333,334 activation of inflammatory mechanisms,335 insulin resistance,336,337 and endothelial dysfunction.338 Other cardiovascular conditions associated with OSA include arrhythmias, HF, MI, and stroke.331,332,339–344 Previous debate about whether OSA is an etiologic factor in hypertension has focused largely around the strong association of OSA with obesity. While obesity is known to contribute in large part to OSA,345-348 patients with OSA may also be at increased risk for weight gain,349 and treatment of OSA may reduce visceral fat.350 It now appears that the potential causal association between OSA and hypertension involves both the obesity-hypertension link and an independent role of OSA in chronic BP elevation. Episodes of apnea with repeated oxygen desaturation in OSA have been shown to stimulate strong sympathetic nervous system discharges that directly elevate BP.333,334 Poorer quality of sleep and shorter sleep periods

may play a reinforcing role in the fatigue and daytime somnolence. Sleep deprivation alone may raise BP351 and impair glucose tolerance.352 There is also a direct relationship between the severity of sleep apnea and the level of BP. Finally, sustained and effective treatment of OSA with continuous positive airway pressure (CPAP) has been reported to lower nighttime and daytime BP in hypertensive individuals with OSA.353–355 In addition to weight loss, improvements in the quality of sleep in OSA patients can occur as a result of a variety of positioning measures during sleep, particularly sleeping on one’s side. Treatment with CPAP can be useful in overall BP lowering and may also improve cardiac ischemia356,357 and HF symptoms.331,332 The role of oral prostheses and surgical approaches remains to be fully defined.354 No specific class of antihypertensive drugs has yet been demonstrated to be superior for BP lowering in OSA patients.354 Hypertension and the Eye Hypertension can affect the retina, choroid, and optic nerve of the eye, particularly with stage 2 hypertension. These changes can be appreciated with inspection of the retinal vessels by direct ophthalmoscopy, photography, or angiography. Hypertensive retinopathy is most commonly manifested by generalized or focal narrowing of retinal arterioles. In acute or advanced hypertension, the retinal vasculature may be injured sufficiently to cause occlusion or leakage. These changes may be manifested as nerve fiber layer infarcts (“soft” exudates or cotton-wool patches), extravascular edema (“hard” exudates), intraretinal hemorrhages, and retinal arterial macroaneurysms. Hypertensive choroidopathy is most frequently seen in young patients with acute hypertension, including cases of eclampsia or pheochromocytoma. Findings include Elschnig spots (nonperfused areas of the choriocapillaris) and Siegrist streaks (linear hyperpigmentation over choroidal arteries). Hypertensive optic neuropathy occurring with severe hypertension may present with flame hemorrhages, optic disc edema, venous congestion, and macular exudates.358–360

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Renal Transplantation Hypertension is a relatively common occurrence in patients receiving organ transplants; in those receiving kidney allografts, the prevalence of hypertension probably exceeds 65 percent.361 Nocturnal hypertension, a reversal of diurnal BP rhythm, may be present in these individuals, who may need ABPM to evaluate overall BP control. Hypertension is less common in other forms of transplantation. The mechanisms of hypertension in transplant patients are multifactorial, but vasoconstriction and long-term vascular structural changes caused by chronic immunosuppressive drugs, which are calcineurin inhibitors (cyclosporin and tacrolimus) and corticosteroids, are among the most important.362 Impaired renal function is another exacerbating factor; despite successful renal transplantation, most patients have enough impairment in renal function to cause relative salt and water retention. Transplant renal artery stenosis may also be a factor. Observational studies suggest that hypertension correlates with deterioration in graft function. Large-scale, controlled, clinical trials on the effects of BP control on decline in GFR or on CVD incidence are lacking in this population. The high risk of graft occlusion and cardiovascular events has suggested that BP should be lowered to 130/80 mmHg or less. Because of the absence of compelling data, no particular class of antihypertensives can be considered superior to any other. The difficulty of lowering BP in this group makes combination drugs necessary in almost all patients. As with other renal diseases, serum creatinine and potassium should be monitored 1–2 weeks following initiation or escalation in therapy with ACEIs or ARBs. A >1 mg/dL increase in serum creatinine should raise the question of renal artery stenosis. Patients With Renovascular Disease Hemodynamically significant renal artery stenosis may be associated with all stages of hypertension, but it is more commonly recognized in patients with stage 2 or resistant hypertension, since these

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are the individuals in whom special evaluation for the problem is carried out. If present bilaterally, renal artery stenosis can lead to reduced kidney function (ischemic nephropathy).363 Clinical clues to renovascular disease include (1) onset of hypertension before age 30 (especially without a family history) or recent onset of significant hypertension after age 55; (2) an abdominal bruit, particularly if it continues into diastole and is lateralized; (3) accelerated or resistant hypertension; (4) recurrent (flash) pulmonary edema; (5) renal failure of uncertain etiology, especially with a normal urinary sediment; (6) coexisting diffuse atherosclerotic vascular disease, especially in heavy smokers; or (7) acute renal failure precipitated by antihypertensive therapy, particularly ACEIs or ARBs.78,79,81 In patients with indications of renovascular disease, captopril-enhanced radionuclide renal scan, duplex Doppler flow studies, and magnetic resonance angiography may be used as noninvasive screening tests. Three-dimensional images can be obtained by spiral computed tomography, a technique that necessitates the use of intravenous contrast.81 Definitive diagnosis of renovascular disease requires renal angiography, which carries some risk, particularly of radiocontrast-induced acute renal failure or atheroembolism.364 In patients, usually women, with fibromuscular dysplasia, results of percutaneous transluminal renal angioplasty (PTRA) have been excellent and comparable to surgical revascularization.365 Patients with normal renal function and atherosclerotic renal artery stenosis that is focal, unilateral, and nonostial also may be managed by angioplasty.365 Renal artery stenting has become an important adjunct to PTRA, being used to counteract elastic recoil and to abolish the residual stenosis often observed after PTRA.366 Even though many patients with high-grade renal artery stenosis remain stable for prolonged periods if BP is well controlled,367 surgical revascularization or PTRA with renal artery stenting may be needed to preserve renal function.81

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Drugs and Other Agents Affecting B lo o d P r e s s u r e

Many prescription drugs and some over-thecounter agents and herbal supplements may affect BP and complicate BP control in treated hypertensive individuals. Consequently, searching for the presence of these agents in a person’s medical history can identify a “secondary” component contributing to BP elevation. Such recognition may negate the need to employ unnecessary and potentially hazardous testing. Use of agents that can affect BP in a given patient should be suspected in the following situations: (1) loss of control of previously well-controlled hypertension; (2) presence of comorbidities (particularly osteoarthritis); (3) biochemical evidence

of intercurrent drug usage (such as an increase in serum potassium or creatinine concentrations with nonsteroidal anti-inflammatory drugs); and (4) atypical hypertension (such as severe but transient hypertension in a young patient presenting with chest pain and ECG changes accompanying possible cocaine usage). Table 24 provides a list of agents that may alter BP. They may affect BP in several ways, such as affecting sodium balance; increasing adrenergic or suppressing parasympathetic neural activity; altering the production, release, or effectiveness of vasoactive hormones; or exerting direct effects on the endothelium or vascular smooth muscle.

Table 24. Common substances associated with hypertension in humans Prescription Drugs Cortisone and other steroids (both cortico- and mineralo-), ACTH Estrogens (usually just oral contraceptive agents with high estrogenic activity) Nonsteroidal anti-inflammatory drugs Phenylpropanolamines and analogues Cyclosporine and Tacrolimus Erythropoietin Sibutramine Ketamine Desflurane Carbamazepine Bromocryptine Metoclopramide Antidepressants (especially venlafaxine) Buspirone Clonidine, BB combination Pheochromocytoma: BB without alpha blocker first; glucagon Clozapine

Street Drugs and Other “Natural Products” Cocaine and cocaine withdrawal Ma Huang, “herbal ecstasy,” and other phenyl propanolamine analogues Nicotine and withdrawal Anabolic steroids Narcotic withdrawal Methylphenidate Phencyclidine Ketamine Ergotamine and other ergot-containing herbal preparations St. John’s Wort Food Substances Sodium chloride Ethanol Licorice Tyramine-containing foods (with MAO-I) Chemical Elements and Other Industrial Chemicals Lead Mercury Thallium and other heavy metals Lithium salts, especially the chloride

ACTH, adrenocorticotropic hormone; BB, beta blocker Note: Bold-faced items within the list represent the substances of more current clinical importance.

Drugs and Other Agents Affecting Blood Pressure

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Alcohol Modest consumption of alcohol (e.g., 30 grams) may lower BP in the first 4 hours after ingestion. Approximately 10–15 hours later (perhaps at the time a patient is seen for an office visit or in the ER during withdrawal), BP increase may be noted. This accounts for some of the discrepancies reported in the literature about alcohol’s effect on BP. The mechanism(s) of alcohol’s effect on BP are unclear but appear predominantly to result from sympathetic neural activation, although changes in cortisol and cellular calcium concentrations also may play a role. Nonaspirin Nonsteroidal Anti-Inflammatory Drugs Nonaspirin nonsteroidal anti-inflammatory drugs (NANSAIDs) represent one of the most common medication classes consumed by hypertensive

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patients. Among the NANSAIDs, older agents like Indomethacin are the most extensively studied. BP responses vary within the class of the NANSAIDs; however, increases in pressure are often accompanied by peripheral edema and weight gain, supporting a salt-retention mechanism of hypertension associated with the loss of natriuretic prostaglandins such as PGE2.368,369 Reduction in the well-described vasodilatory effects of some prostaglandins are another mechanism. Cyclooxygenase-2 (COX-2) inhibitors also may cause elevation in BP.370–372 Recently, a double-blind randomized trial was conducted evaluating the effects of celecoxib, rofecoxib, and naproxen on 24-hour BP in type 2 diabetic patients with osteoarthritis whose hypertension was treated with ACEIs or ARBs. At equally efficacious doses for the management of osteoarthritis, treatment with rofecoxib (but not celecoxib or naproxen) induced a significant increase in average 24-hour SBP in type 2 diabetic patients receiving ACEIs or angiotensin-II receptor blockers.373 Thus, current data suggest that certain NSAIDs and COX-2 inhibitors may have destabilizing effects on BP control in diabetic hypertensive patients. This is a major concern because diabetic patients are often older and obese, and both obesity and aging predispose to osteoarthritis as well as diabetes.

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Improving Hypertension Control

Issues Dealing With Adherence to Regimens

Clinical Inertia

Behavioral models suggest that the most effective therapy prescribed by the most careful clinician will control hypertension only if the patient is motivated to take the medication as directed and to establish and maintain a health-promoting lifestyle. Motivation improves when patients have positive experiences with, and trust in, their clinicians. Better communication improves outcomes; empathy builds trust and is a potent motivator (table 25).374

There is a broad range of clinician commitment to optimal hypertension therapy (table 26). Failure to titrate or combine medications and to reinforce lifestyle modifications, despite knowing that the patient is not at goal BP, represents clinical inertia which must be overcome. This may be due in part to clinician focus on relieving symptoms, a lack of familiarity with clinical guidelines, or discomfort in titrating to a goal.376 Table 26. Clinician awareness and monitoring

Table 25. Provide empathetic reinforcement ■

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Adopt an attitude of concern coupled with hope and interest in the patient’s future. Provide positive feedback for blood pressure and behavioral improvement. If blood pressure is not at goal, ask about behaviors to achieve blood pressure control. Hold exit interviews to clarify regimen. A patient may tell you that they understand but tell the exit interviewer that they do not. Schedule more frequent appointments and health care personnel contact with patients who are not achieving goal blood pressure.

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What Can the Clinician Do? Clinician-patient partnerships that are based on trust, respect, and a holistic knowledge of the patient correlate with positive outcomes of care, such as adherence, satisfaction, and improved health status. Patients often evaluate a clinician’s competence by their customer service skills, not their clinical skills.375 Customer service includes ease of access, minimal waiting time, and a positive regard from the office staff; all are known to influence provider satisfaction and patient adherence. Clinicians are the role model and should train staff by providing a positive, interactive, empathetic environment. This will increase patients’ comfort and willingness to participate in their own care.

Anticipate adherence problems for young men. Consider nonadherence as a cause of: • Failure to reach goal blood pressure • Resistant hypertension • Sudden loss of control. Encourage patients to bring in all medications from all physicians and other sources, whether prescription, complementary, or over-the-counter, to each visit for review and to rule out iatrogenic causes of elevated blood pressure. Ask what the patient takes for pain. Recognize depression and other psychiatric illnesses, including panic attacks, and manage appropriately. Be willing to change unsuccessful regimens and search for those more likely to succeed.

A number of approaches are available to overcome clinical inertia. One of the most effective is to use decision support systems that prompt theclinician to advance therapy when a goal has not been achieved (table 27). Such systems can be electronic (computer- or personal digital assistantbased) or paper-based (flow charts, algorithms, guidelines). Feedback reminders from any source (computer-based, automated telephone-based, nurse care managers, outside auditors) can be very effective in not only helping to achieve BP goals but to alert clinicians to missed patient appointments, necessary prescription refills, and laboratory abnormalities.377

Improving Hypertension Control

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Table 27. Organize care delivery systems ■ ■

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Schedule next appointment before patient leaves office. Use appointment reminders, preferably computer-based, and contact patients to confirm appointments. Follow up with patients who missed appointments. Use an office-based system approach for monitoring and followup (e.g., educate staff to provide patient encouragement, computer or chart reminders, disease management aids).

Patient-centered behavioral interventions, such as counseling, improve BP control (table 28).378 Nurse clinicians and pharmacists have proven their effectiveness in helping to achieve goal BP.379 Commercial health plans may provide resources for chart auditing or other assistance to improve BP control.380 Clinicians should periodically audit their own patient files to assess their degree of compliance and success with established goals and treatment interventions. Table 28. Patient education about treatment ■

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Assess the patient’s understanding and acceptance of the diagnosis of hypertension. Discuss patient’s concerns, and clarify misunderstandings. Tell the patient the blood pressure reading, and provide a written copy. Come to agreement with the patient on goal blood pressure. Ask the patient to rate from 1 to 10 his or her chance of staying on treatment. Inform the patient about recommended treatment, and provide specific written information about the role of lifestyle including diet, physical activity, dietary supplements, and alcohol intake; use standard brochures when available. Elicit concerns and questions, and provide opportunities for the patient to state specific behaviors to carry out treatment recommendations. Emphasize: • Need to continue treatment • Control does not mean cure • One cannot tell if blood pressure is elevated by “feeling or symptoms”; blood pressure must be measured.

have the information they need to reliably assess quality of health care (http://www.ncqa.org/Programs/HEDIS). Enforcement of HEDIS guidelines by managed care organizations has successfully increased the appropriate use of ACEIs in HF and of BBs in patients who have suffered an MI. NCQA now monitors physician records for the percent of patients whose BP is